The general objectives of this research project are to show that (1) increased concentrations of oxygen at normal atmospheric pressures induce biochemically measurable changes in the newborn mouse lung in vivo, such as acute and chronic inhibition of DNA synthesis, (2) such changes directly relate to the increased oxygen concentration and duration of exposure, (3) and that the injury induced by oxygen toxicity is manifested by damage to the bronchiolar mucosal cells. This coming year we intend to (1) continue the characterization of the recovery from acute, subacute, and chronic exposure to 100 per cent oxygen (2) continue the identification autoradiographically of the major cellular regions involved in the recovery from DNA synthesis inhibition, (3) continue the electromicroscopic comparison of human infant lung exposed to high concentrations of oxygen with the newborn mouse lungs similarly exposed, (4) begin identification of the specific cell types most sensitive to the acute inhibition of DNA synthesis (5) begin the characterization of collagen deposition in the lung resulting from continuous exposure to 100 per cent oxygen and (6) begin the evaluation of superoxide dismutase as a potential protective agent for pulmonary oxygen toxicity. Bibliographic references: Bonikos, D.S., Bensch, K.G., Ludwin, S.K., Northway, W.H., Jr.,: Oxygen toxicity in the newborn: The effect of prolonged 100 per cent O2 exposure on the lungs of newborn mice. Laboratory Investigation, Vol. 32, No. 5, p. 619, 1975. Schober, R., Bensch, K.G., Kosek, J.C., Northway, W.H.: On the origin of the membranous intraalveolar material in pulmonary alveolar proteinosis. Experimental and Molecular Pathology 21, 246-258 (1974).